Early last week we told you about a new paper published in the Quarterly Review of Biology which suggests that homosexuality arises on account of epigenetic processes rather than genetic ones (i.e. non-heritable factors that alter the expression of DNA). Not surprisingly, the web exploded in a firestorm of debate, with opinions and interpretations spanning the entire spectrum. Now, writing in Lost in Transcription, evolutionary biologist Jon Wilkins clears up some misconceptions about the study, saying that most people simply read far too much into it.

As Wilkins points out, the researchers William Rice, Urban Friberg, and Sergey Gavrilets, presented a potential model to explain homosexuality — what was a really only a theory paper. They didn't actually prove anything, nor was any direct correlation shown between their hypothesized epigenetic mechanism and the emergence of homosexuality. Wilkins writes:

That's not to say that this is a bad paper. In fact, it's a very good paper. The authors integrate a lot of different information to come up with a plausible biological mechanism for epigenetic modifications to exert influence on sexual preference. They demonstrate that such a mechanism could be favored by natural selection under what seem to be biologically realistic conditions. Most importantly, they formulate their model into with clear predictions that can be empirically tested.

But those empirical tests have not been carried out yet. And, in biology, when we say that a paper shows that X causes Y, we generally mean that we have found an empirical correlation between X and Y, and that we have a mechanistic model that is well enough supported that we can infer causation from that correlation. This paper does not even show a correlation. It shows that it would probably be worth someone's time to look for a particular correlation.

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Wilkins then shows how the researchers sought to explain homosexuality by considering "epi-marks" — the idea that there must be some epigenetic differences between male and female fetuses that "encode differential sensitivity" to some kind of external factor in the womb, namely testosterone. He writes:

All of this seems well reasoned, and is supported by the review of a number of studies. It is worth noting, however, that we don't, at the moment, know exactly which sex-specific epigenetic modifications these would be. One could come up with a reasonable list of candidate genes, and look for differential marks (such as DNA methylation or various histone modifications) in the vicinity of those genes. However, this forms part of the not-yet-done empirical work required to test this hypothesis, or, in the journalistic vernacular, "show" that this happens.

Indeed, as Wilkins correctly points out, many journalists jumped the gun on the study and made too many presumptions about what, exactly, the researchers were claiming. He suspects it was the grossly oversold press release from NIMBios, and concludes by saying:

If you know that this is a pure theory paper, this is maybe not misleading. Maybe. But phrases like "solves the evolutionary riddle of homosexuality" and "finding that . . . epi-marks . . . cause homosexuality in opposite-sex offspring," when interpreted in the standard way that I think an English speaker would interpret them, pretty strongly imply things about the paper that are just not true.